Chapter 046. Sodium and Water (Part 7)

Diagnosis(Fig. 46-1) Hyponatremia is not a disease but a manifestation of a variety of disorders. The underlying cause can often be ascertained from an accurate history and physical examination, including an assessment of ECF volume status and effective circulating arterial volume. The differential diagnosis of hyponatremia, an expanded ECF volume, and decreased effective circulating volume includes congestive heart failure, hepatic cirrhosis, and the nephrotic syndrome. Hypothyroidism and adrenal insufficiency tend to present with a near-normal ECF volume and decreased effective circulating arterial volume. All of these diseases have characteristic signs and symptoms. Patients with SIADH are usually euvolemic.Figure 46-1Algorithm...
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Chapter 046. Sodium and Water (Part 7) Chapter 046. Sodium and Water (Part 7) Diagnosis (Fig. 46-1) Hyponatremia is not a disease but a manifestation of a variety ofdisorders. The underlying cause can often be ascertained from an accurate historyand physical examination, including an assessment of ECF volume status andeffective circulating arterial volume. The differential diagnosis of hyponatremia,an expanded ECF volume, and decreased effective circulating volume includescongestive heart failure, hepatic cirrhosis, and the nephrotic syndrome.Hypothyroidism and adrenal insufficiency tend to present with a near-normal ECFvolume and decreased effective circulating arterial volume. All of these diseaseshave characteristic signs and symptoms. Patients with SIADH are usuallyeuvolemic. Figure 46-1 Algorithm depicting clinical approach to hyponatremia. ECF,extracellular fluid; SIADH, syndrome of inappropriate antidiuretic hormonesecretion. Four laboratory findings often provide useful information and can narrowthe differential diagnosis of hyponatremia: (1) the plasma osmolality, (2) the urineosmolality, (3) the urine Na+ concentration, and (4) the urine K+ concentration.Since ECF tonicity is determined primarily by the Na+ concentration, mostpatients with hyponatremia have a decreased plasma osmolality. The appropriaterenal response to hypoosmolality is to excrete the maximum volume of diluteurine, i.e., urine osmolality and specific gravity of 100 mosmol/kg). Patientsare typically normovolemic and have normal Na+ balance. They tend to be mildlyvolume-expanded secondary to water retention and have a urine Na + excretion rateequal to intake (urine Na+ concentration usually >40 mmol/L). By definition, theyhave normal renal, adrenal, and thyroid function and usually have normal K + andacid-base balance. SIADH is often associated with hypouricemia due to theuricosuric state induced by volume expansion. In contrast, hypovolemic patientstend to be hyperuricemic secondary to increased proximal urate reabsorption. Hyponatremia: Treatment The goals of therapy are twofold: (1) to raise the plasma Na + concentrationby restricting water intake and promoting water loss and (2) to correct theunderlying disorder. Mild asymptomatic hyponatremia is generally of little clinicalsignificance and requires no treatment. The management of asymptomatichyponatremia associated with ECF volume contraction should include Na+repletion, generally in the form of isotonic saline. The direct effect of theadministered NaCl on the plasma Na+ concentration is trivial. However,restoration of euvolemia removes the hemodynamic stimulus for AVP release,allowing the excess free water to be excreted. The hyponatremia associated withedematous states tends to reflect the severity of the underlying disease and isusually asymptomatic. These patients have increased total body water that exceedsthe increase in total body Na+ content. Treatment should include restriction of Na+and water intake, correction of hypokalemia, and promotion of water loss inexcess of Na+. The latter may require the use of loop diuretics with replacement ofa proportion of the urinary Na+ loss to ensure net free-water excretion. Dietarywater restriction should be less than the urine output. Correction of the K + deficitmay raise the plasma Na+ concentration by favoring a shift of Na+ out of cells asK+ moves in. Water restriction is also a component of the therapeutic approach tohyponatremia associated with primary polydipsia, renal failure, and SIADH(Chap. 334). The recent development of nonpeptide vasopressin antagonists hasintroduced a new selective treatment for euvolemic and hypervolemichyponatremia.